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Infection and Immunity, March 2003, p. 1370-1378, Vol. 71, No. 3
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.3.1370-1378.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Primed Peritoneal B Lymphocytes Are Sufficient To Transfer Protection against Brugia pahangi Infection in Mice

Natalia Paciorkowski,1 Leonard D. Shultz,2 and T. V. Rajan1*

Department of Pathology, University of Connecticut Health Center, Farmington, Connecticut 06030-3105,1 The Jackson Laboratory, Bar Harbor, Maine 046092

Received 11 September 2002/ Returned for modification 16 October 2002/ Accepted 25 November 2002

Lymphatic filariasis is a tropical disease caused by the nematode parasites Wuchereria bancrofti and Brugia malayi. Whereas the protective potential of T lymphocytes in filarial infection is well documented, investigation of the role of B lymphocytes in antifilarial immunity has been neglected. In this communication, we examine the role of B lymphocytes in antifilarial immunity, using Brugia pahangi infections in the murine peritoneal cavity as a model. We find that B lymphocytes are required for clearance of primary and challenge infections with B. pahangi third-stage larvae (L3). We assessed the protective potential of peritoneal B lymphocytes by adoptive transfer experiments. Primed but not naïve peritoneal B cells from wild-type mice that had been immunized with B. pahangi L3 protected athymic recipients from challenge infection. We evaluated possible mechanisms by which B cells mediate protection. Comparisons of cytokine mRNA expression between B-lymphocyte-deficient and immunocompetent mice following B. pahangi infection suggest that B cells are required for the early production of Th2-type cytokines by peritoneal cells. In addition, B-cell-deficient mice demonstrate a defect in inflammatory cell recruitment to the peritoneal cavity following B. pahangi infection. The data demonstrate a critical role of B lymphocytes in antifilarial immunity in naïve mice and in the memory response in primed mice.

* Corresponding author. Mailing address: Department of Pathology, University of Connecticut Health Center, 263 Farmington Ave., Farmington, CT 06030-3105. Phone: (860) 679-3221. Fax: (860) 679-2936. E-mail: rajan{at}neuron.uchc.edu.

Editor: W. A. Petri, Jr.

Infection and Immunity, March 2003, p. 1370-1378, Vol. 71, No. 3
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.3.1370-1378.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Rajan, B., Ramalingam, T., Rajan, T. V. (2005). Critical Role for IgM in Host Protection in Experimental Filarial Infection. J. Immunol. 175: 1827-1833 [Abstract] [Full Text]  
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  • Abraham, D., Leon, O., Schnyder-Candrian, S., Wang, C. C., Galioto, A. M., Kerepesi, L. A., Lee, J. J., Lustigman, S. (2004). Immunoglobulin E and Eosinophil-Dependent Protective Immunity to Larval Onchocerca volvulus in Mice Immunized with Irradiated Larvae. Infect. Immun. 72: 810-817 [Abstract] [Full Text]  
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